This project deals with the regulation of metabolism and proliferation of early embryos. The overall aim is to determine the means by which mouse blastocysts are maintained in a quiescent state during delayed implantation. Two basic hypotheses concerning this control will be explored: 1) that embryonic dormancy is maintained through the limitation in the uterus of some components essential for normal metabolic function; and 2) that dormancy is maintained by the inhibitory action of a specific uterine component. The first possibility will be tested by assessing the effects of limited concentrations of ions comprising a simple defined medium which supports in vitro activation of dormant embryos. A reversible prevention of activation with limited amounts of a particular component, will suggest a mechanism by which quiescence may be maintained in vivo. The second possibility will be investigated by testing the effects of uterine extracts on the in vitro activation process. Maintainance of a reversible dormancy by these extracts will indicate a possible role of an inhibitory factor operating in vivo. If this appears to be the case, the inhibitory component will be purified and characterized by standard biochemical techniques. The physiological role of this factor will be assessed by determining its presence in uterine fluid, establishing its hormone dependency, determining the effect of the factor on various indices of embryo metabolism, examining the ability of this component to induce quiescence in active embryos, and investigating its species and tissue specificity. This study will provide valuable information on the embryo-uterine interaction involved in controlling early embryo development and implantation.